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Genome structure

Retroshuffling the genomic deck

Nature volume 398, pages 109–111 (1999)Cite this article

The process of 3′ transduction may occur in many eukaryotes, and several possible examples of it have been reported. In the most convincing case, a progenitor human L1 element, which spawned an insertion mutation in the dystrophin gene, was identified based on its unique, transduced 3′ flanking sequence tag4. A more ancient event, involving a human CFTR exon, probably occurred around ten million years ago5. In mouse cells, an L1 read-through RNA has been found associated with ribonucleoprotein particles6. And the structure of a Drosophila gene, jingwei, was proposed to arise from insertion of the complementary DNA for an alcohol dehydrogenase gene into an unrelated gene7. There are no retrotransposon sequences in jingwei, but its structure is consistent with a 3′ transduction event in which reverse transcription terminated before retrotransposon sequences were reached (Fig. 1a).

Retroviruses can incorporate cellular genes into their genomes, probably by aberrant read-through transcription into adjacent host DNA. But L1 elements differ from retroviruses in that they do not form the precise 3′ ends that are normally specified by retroviral long-terminal repeats. The signal for 3′ end formation comes instead from cleavage/polyadenylation signal sequences. Although the human L1 element contains a putative polyadenylation signal near its 3′ end, its sequence is not optimal — if it functions at all. This weak polyadenylation signal is supposedly suppressed by the action of more potent polyadenylation signals in the flanking DNA, resulting in the formation of a read-through transcript which could then act as the template for reverse transcription4, 8. By this hypothesis, the nature of the flanking DNA dictates which 3′ end gets formed. This built-in sloppiness has rendered L1 an efficient exon-mobilizing machine.

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Figure 1: Mechanism of 3′ transduction by the L1 retrotransposon, based on the results of Moran et al.2.
Figure 2: Evolutionary consequences of L1-mediated 3′ transduction.

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  1. Oxana K. Pickeral

    Present address: the National Center for Biotechnology Information, National Institutes of Health, Bethesda, 20894, Maryland, USA

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  1. The Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, 21205, Maryland, USA

    Jef D. Boeke

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  1. Jef D. Boeke
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Boeke, J., Pickeral, O. Retroshuffling the genomic deck. Nature 398, 109–111 (1999). https://doi.org/10.1038/18118

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